The Objective of theses Blogs -created by Prof.Garfia.A- is show the most representative and illustrative cases which I have found during 25 years of experience in the field of the Forensic Pathology in Spain, in order to use this experience to the service of the younger people who wish to obtain a Medical Degree in Forensic Pathology.Also I intend that this information can be useful to the professional people who are working, daily, to the Justice Service in Spain.

sábado, 18 de abril de 2009

18.-FATAL OBSTRUCTIVE EDEMA OF THE ARITENOEPIGLOTTIC FOLDS FOLLOWING AN ANAPHYLACTIC REACTION IN A ASMATHIC PATIENT.

PROF.GARFIA.A

Fatal upper airway obstruction can occurs in children and in adults people. In young children is most commonly caused by inhaled foreing bodies, particularly due to food or toy parts. Much less frequently fatal compromise of the superior airway occurs due to an congenital malformation such as a lingual thyrod at the base of the tongue (see:http://www.forensic-histopathology-garfiaa.blogspot.com), from the same author), or a lingual thyroglossal duct cyst. Acquired lesions may also result in fatal airway narrowing and often involve an infectious etiology such as acute epiglottitis, or acute inflamation of a lingual tonsil. Many of these cases occurs in infancy and very early chilhood, although food aspiration, so called "cafe coronary death" may occur at any age. A special chapter in adults it is referred to deaths due to Anaphylactic Reactions after insect bites - wasp, hornets and bees- or deaths following drug administration sometimes difficult to diagnostised due to some drugs are drugs normally utilized againts the anaphylactic process, such as metilprednisolone or other corticoids which utilize "carboximethylcellulose" as disolvent.

CASE REPORT

A finnish man, 58 years old, with pathological antecedents of alergical illnes, arterial hypertension and bronchial asthma presented an undiagnosed clinical picture of pain in the right half of the face, accompanied by important facial and lingual edema. Soon after, the patient went to the Hospital Emergency Service and, after 3 hours, transferred to Intensive Care Unit, where he suffered cardiorespiratory arrest and die.

The medicament treatment guide was the following:

At Home

Urbason....60mg.i.v.

Amoxicillin..875 mg/12 hours.

Antihistamines...(unknown).

Few hours later the clinical picture suffers progresive worsening and the patient go to the Urgency Hospital Service.At the Hospital, the patient presented severe lingual and laringeal edema.The Medical team administrated:

Actocortin...300mg+

Urbason......40 mg,dissolved in a 100ml ampoule of physiological serum. After that, the patient presented a convulsive picture and cardiorespiratory arrest and was sended to the Critic Unit.The orotracheal intubation with a Sheridan tube number 6, was not possible.The patient received the following medication:

Adrenalin: two bolus of 20mg.

Atropine......3mg.

Salbutamol. 3mg

The patient went to cardiovascular arrest and die after 70 min. of cardiopulmonary resuscitation.

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Photo nº 1.-Macroscopical aspect of the larynx, posterior aspect. To note thesevere obstructive edema (arrows) of the arytenoepiglottic folds (stars)and the erasure of the cuneiform and corniculate tuberclesof the right sidedue to the brutal suffocating edema, typical of the larynx anaphylactic response.The differential dignosis must be made with the infectious acute fatal epiglottitis, where the affectation of the inflamation affects, more specifically, to the epiglottical structures.Prof.Garfia.A

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PHOTO Nº 2.To show the microscopical aspect of the arytenoepiglottic folds.Note that the inflamation is due to the edema with scanty cellular componente inside it. This is the second characteristic of the anaphylactic affectation of the larinx(anaphylactic target organ in asthmatic people). Ep=epithelium. Ed= edema.Prof.Garfia.A

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PHOTO Nº 3.- To show the scanty cellular component (arrows) inside the edema in the anaphylactic reaction. Cells are, principally, leucocytes eosinophiles and plasma cells (the third characteristic of the laringeal anaphilactic reaction). Masson Trichrome-stain.Prof.Garfia.A

jueves, 2 de abril de 2009

17.-SUDDEN CARDIAC DEATH DUE TO SEVERE CORONARY ATHEROSCLEROSIS IN A YOUNG MAN -26 YEARS OLD.PROF. GARFIA.ACASE REPORT

A 26 year old patientwho died as a consequence of myocardial infarction in the presence of witnesses.Two weeks earlierhe had visited his family doctor for pain in his shoulder and left arm, which was diagnosed as muscular strain for which the patient was recommended to place his arm in a sling. The pathological study showed the existence of a myocardial infarct in the interventricular septum and the scar was two weeks old.The left circumflex coronary and the anterior descending arteries, presented severe atheromatous stenosis, of more than 90%. Among the points of interest in the family history, the existence of two episodes of myocardial infarction with hospitalization in the Intensive Care Unit of the victim's elder brother, aged 32 years, due to a myocardial infarct and the death of a first cousin 28 years old - also due to myocardial infarction - were significant. Given the youth of the deceased and his family history, the convenience of carrying out a lipid study was suggested to the family, in view of the suspicion of possible familial hiperlipidaemia.The results of the autopsy, together with the familiy history, the biochemical and the lipid study carried out pointed to the existence of aCombined Primary Familial Hiperlipidaemia. Other possibility to explain the severe atheromatous lesions found in this case would be the existence of an abnormal elevation of Lipoprotein (a) ( > 0.3 g/L), - considered by numerous authors an independent risk factor to have conditioned the apparition of a severe atherosclerotic coronariopathy and sudden cardiac death in young people- was unfortunatelly not determined in this case.

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Photo 1.- 26 year old patient. The left anterior descending coronary arteryshowing severe lumen narrowing due to coronary atherosclerosis (arrow). The red line inside the artery show the residual arterial lumen.Prof.Garfia.A

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Photo 2.-Microscopical aspect of the same arteryshowing the severe narrowing of the lumen ( more of 90%) due to the existence of a fibroatheromatous plaque with fibrin deposition (arrows), probably dependent of the organization of a previous trombus(L=lumen).Prof.Garfia.A

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Photo 3.- Microscopical section of the left circumflex coronary arteryshowing a severe narrowing of the lumen due to the existence of a typical fibrous cap atheroma which contains a necrotic core containing cholesterol clefts, foam cells and fibrous tissue.Prof.Garfia.A

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Photo 4.- Right coronary artery.It shows intimal hyperplasia -with fibrous tissue and foam cells- but the reduction of the arterial lumen (L) is not so severe than in the others coronaries arteries.Focal preatheromatous lesion.Prof.Garfia.A

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Photo nº.-5.- Showing an intramyocardial arteriolewhich presents a thicker muscular wall -and penetration of connective tissue from the adventitia- for the age of the patient.Prof.Garfia.A

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Photo nº.6.- This section of the heart shows the localization of themyocardial infarct (arrows) in the interventricular septum.Prof.Garfia.A

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Photo nº. 7.- The mycroscopical study of this area demonstrated the existence of a myocardial infarct-aproximatelly two weeks old- due to the presence of granulation tissue plenty of macrophages cells with cellular debris and neocollagen fibers formation. (IAM= myocardial infarct). Prof.Garfia.A